CASE REPORT/CLINICAL TECHNIQUES

Saurabh Mannan, BDS, DMD,

Dental Abscess to Septic MPH, MS,* Patricia A. Tordik,
DMD,* Frederico C. Martinho,
Shock: A Case Report and DDS, MSc, PhD,* Noah Chivian,
DDS,† and Craig S. Hirschberg,
Literature Review DDS†

ABSTRACT
SIGNIFICANCE
Sepsis is a leading cause of death in the United States, with a mortality rate in excess of
215,000 deaths per year. It may lead to septic shock, a complex pathophysiological process This is a report of a healthy 23-
with microbial and host response events that progress to multisystem derangement. There is year-old male who presented
poor documentation of the relationship between dental infection and septic shock, with only a to the urgent care clinic of a
few case reports of septic shock secondary to dentoalveolar abscess. Presented is a case of dental school for treatment of
sepsis/septic shock in a 23-year-old man with signs and symptoms of pulpal necrosis, acute an endodontic and canine
apical abscess, and canine space infection that rapidly progressed to an altered mental state, space infection. The patient’s
hyperthermia, tachycardia, hypotension, acute respiratory failure, diarrhea, renal insufficiency, condition rapidly deteriorated
lactic acidosis, leukocytosis, and hyperglycemia. Once septic shock develops, the mortality to a medical emergency and
rate is nearly 50%. Early antimicrobial intervention is associated with surviving severe sepsis, near-death experience
making it critical for dentists to understand local factors leading to the crisis and the signs and because of sepsis and septic
symptoms of the sepsis–septic shock continuum. (J Endod 2021;47:663–670.) shock. Significant changes in
vital signs are not expected in
KEY WORDS localized infections. Hence, all
Bacteremia; dentoalveolar abscess; odontogenic infection; sepsis; septic shock vital signs should be routinely
checked while examining
infected dental patients.
Sepsis is a serious, complicated medical condition with a high mortality rate. Sepsis and septic shock
are 2 entities occurring as a continuum, with sepsis leading to septic shock1. Sepsis was first defined
in 1991 as a systemic inflammatory response syndrome due to suspected infection with 2 or more
specified clinical criteria. Septic shock includes hypotension and organ dysfunction that persists
despite volume resuscitation, along with the systemic inflammatory response syndrome criteria2.
Using these definitions, the Surviving Sepsis Campaign developed guidelines for a protocol-driven
model of care3. In 2016, the international Sepsis-3 Committee defined sepsis as “a life-threatening
condition caused by a dysregulated host response to infection, resulting in organ dysfunction,”
whereas septic shock is “circulatory, cellular, and metabolic abnormalities in septic patients,
presenting as fluid-refractory hypotension requiring vasopressor therapy with associated tissue
hypoperfusion (lactate . 2 mmol/L)”4.
In the United States, the incidence of severe sepsis is estimated to be 300 cases per 10,000
population5, with over 30 million cases of sepsis/annum estimated worldwide6. More than 500,000 From the *Endodontics Division,
annual emergency department visits in the United States are related to sepsis7. In 2013, sepsis-related Department of Advanced Oral Sciences
illness was the most expensive reason for hospitalization, costing $23.7 billion8. One study reported the and Therapeutics, University of Maryland
mortality rate of sepsis as 33%–35%9, whereas hospital deaths in patients with sepsis from 2 School of Dentistry, Baltimore, Maryland;
and †Department of Endodontics,
independent cohorts found mortality ranged between 34%–56%10,11. With sepsis-related mortality Rutgers School of Dental Medicine,
above 215,000 deaths per year, it is a leading cause of death in the United States6. Newark, New Jersey
In 2013, New York state was the first to implement regulations that require hospitals to follow
Address requests for reprints to Dr
protocols for treating sepsis, which resulted in a greater decrease in sepsis mortality compared with Patricia A. Tordik, Endodontics Division,
control states without regulations12. Illinois, New Jersey, and Indiana also have mandatory practices, Department of Advanced Oral Sciences
whereas other states have introduced bills into legislature as recently as 2020 or use voluntary and Therapeutics, University of Maryland
School of Dentistry, 650 W Baltimore
programs13. In 2018, Maryland developed a public awareness campaign to help prevent sepsis
Street, Baltimore, MD 21201.
fatalities14. E-mail address: ptordik@umaryland.edu
We report a case of an urgent care visit to a dental school clinic for treatment of an endodontic and 0099-2399/$ - see front matter
canine space infection that quickly escalated to a medical emergency and near-death experience for the Copyright © 2021 American Association
patient because of sepsis and septic shock. of Endodontists.
https://doi.org/10.1016/
j.joen.2020.12.016

JOE  Volume 47, Number 4, April 2021 Dental Abscess to Septic Shock 663
CASE REPORT
Day 1
0900 Hours
A 23-year-old man presented to the
predoctoral urgent care clinic with a chief
complaint of an ongoing “toothache and
severe pain.” His past medical history was
noncontributory with no known drug allergies;
his past dental history included caries in tooth
#7. The patient was taking acetaminophen. His
vital signs are provided in Table 1. A limited oral
examination revealed pulpal necrosis/acute
apical abscess in tooth #7. For pain
management, 1 cartridge of lidocaine with
1:100,000 epinephrine (34 mg lidocaine
hydrochloride/0.017 mg epinephrine) mesial
and distal to the infected area was
administered using a standard local infiltration
technique.
1030 Hours
A dental student was assigned to initiate root
canal treatment of tooth #7 in the predoctoral
endodontics clinic later the same day. With
pain relief, the patient planned to hydrate and
eat a light meal before his appointment.
1415 Hours
The patient presented to the predoctoral
endodontics clinic. Despite having a toxic
appearance, he was alert; was oriented to
person, place, time, and situation; and was in
no respiratory distress. The attending faculty
made a cursory diagnosis of canine space
infection and immediately transferred care to
the on-call postgraduate endodontic resident.
1430 Hours
His past medical and dental history was
reviewed, medications were reconciled, and
no known drug allergies was noted. His vital
signs are presented in Table 1. The clinical/
radiographic data are provided in Table 2. A
periapical radiograph was provided by the
urgent care clinic (Fig. 1). The patient said he
felt cold and was given a blanket.
1440 Hours
Within 10 minutes of evaluation, intense
shivering ensued. The patient was lethargic
and hyperthermic. His tympanic temperature
and vital signs are presented in Table 1.
Emergency medical service (EMS) was
activated. Until the paramedics arrived, the
patient was semireclined, his airway was
maintained, respiration was supported with
100% oxygen, and ice packs were applied to
the forehead and axillae. The patient became
tachypneic, difficult to arouse, and lost
consciousness after EMS arrival. Because of
the suspected contribution of the dental
infection, the attending endodontist requested
the patient be transported to the university
hospital emergency department (ED), where
there is an oral and maxillofacial surgery
service, rather than to the city hospital on call.
The ED consented to accept the patient.
Tachycardia was refractory to 6 mg adenosine
provided en route to the ED. His vital signs are
recorded in Table 1. A review of his systems
are included in Table 3.
1810 Hours
The patient was sedated with propofol and
benzodiazepine and then intubated to protect
the airway. A full-body computed tomographic
scan was ordered because of the sudden
alteration in mental awareness. The differential
diagnosis included meningitis, encephalitis,
septic encephalopathy, toxin/ingestant, and
seizure/postictal. The immediate treatment
plan was for magnetic resonance imaging and
electroencephalography while awaiting the
results of urodynamic studies and lumbar
puncture. To manage possible infection, the
patient was given intravenous cefepime,
vancomycin, and metronidazole, which was
later changed to ceftriaxone, vancomycin,
metronidazole, and acyclovir. A lactated Ringer
solution bolus was administered for fluid
replenishment.
2334 Hours
The patient had elevated troponin, lactate, and
creatinine values (Table 3). Primary cardiac
pathology was considered not likely,
transthoracic echocardiography was planned,
and the patient was admitted to the critical
care resuscitation unit.
Day 2
Approximately 8 hours after admission, the
working diagnosis included septic shock,
central nervous system failure or compromise,
metabolic crisis, acute respiratory failure, renal
insufficiency, elevated liver enzymes,
leukocytosis, and fever. The transthoracic
echocardiographic finding was tachycardia
secondary to sepsis, volume depletion, and
fever. Heart rate decreased with volume
resuscitation, leading to the conclusion of
sinus tachycardia. Norepinephrine bitartrate
(Levophed; CIBA, Basel, Switzerland) was
administered to maintain a mean arterial
pressure .65 mm Hg based on the bedside
echocardiogram suggesting myocardial
dysfunction and euvolemia. Full ventilator
support continued until vast improvement
allowed for extubation. Findings of
reconstructed computed tomographic
images, taken with contrast to evaluate for
infection, were unremarkable (Table 4).

TABLE 1 - Vital Signs as Recorded in the Medical Record

Temperature MAP
Day Time BP Pulse (beats/min) HR R (Rate) R (Rhythm) R (Depth) SpO2 % ( F) Temp ( C) (mm Hg) Arterial BP
1 0900 155/96* 80 12 Regular Normal
1 1430 170/104* 100* 12 Regular Normal
1 1440 170/100* 160* 18* Increased Shallow 106* 41.1*
1 1533 135/98* 183* 174* 20* Increased Shallow 97* 102.9* 39.4*
1 1931 113/66 128* 114* 20* Increased Shallow 100 100* 37.8*
2 0200 95/54* 79 75 15 Regular Normal 100 98.6 37* 67.67* 114/53

BP, blood pressure; HR, heart rate; MAP, mean arterial pressure; R, respiration; SpO2, oxygen saturation.
*Values outside of the normal range.

TABLE 2 - Clinical and Radiographic Data Collection

Lymphadenopathy upon Mobility Probing Periapical

Tooth Swelling palpation ST Cold Hot EPT Percussion Palpation (mm) (mm) radiolucency (mm)
7 V, CS N N NR NT NT S S 0 ,3 6!8

CS, canine space; EPT, electric pulp test; N, none; NR, no response; NT, not tested; S, sensitive; ST, sinus tract; V, vestibular.

664 Mannan et al. JOE  Volume 47, Number 4, April 2021

Day 3
The oral and maxillofacial surgery service
completed a head/neck examination. Extraoral
swelling with obliteration of the nasiolabial fold
and a broad, fluctuant swelling in the vestibule
were noted. A diagnosis of acute apical
abscess/canine space infection associated
with tooth #7 was made. After infiltrating with
lidocaine/epinephrine, a vestibular, horizontal
incision was made extending from tooth #6 to
tooth #8. Subperiosteal blunt dissection
produced purulent and sanguineous drainage.
Tissues were irrigated with a high volume of
0.9% normal saline, and a gauze pressure
dressing was placed.

Day 4
An improvement in fever, leukocytosis, and
hemodynamics was noted. The clinical course
of infection was improving.

Day 5
The patient was discharged to home with a
7-day course of amoxicillin/clavulanate
potassium 875 mg and 30 mL 0.12%
chlorhexidine gluconate oral rinse. He was
advised to follow up with the dental school,
where the nonsurgical root canal treatment FIGURE 1 – The periapical radiograph provided by the urgent care clinic.
was completed by the same predoctoral
TABLE 3 - A Review of the Systems and Pertinent Values from the Comprehensive Metabolic Panel
student, 3 months later (Fig. 2). The discharge
note stated the following: “Because of likely
Normal findings Abnormal findings
dental abscess, the patient was hypotensive
on presentation and showed signs of ischemic General Febrile, altered mental status:
nonverbal, agitated, incoherent
end organ damage with lactic acidosis,
Skin Diaphoretic
transaminitis, troponinemia, acute kidney injury
Head and neck No traumatic head injury or cervical
and altered mental status (AMS), requiring lymphadenopathy
intubation.” Pulmonary/chest No stridor or wheezes Tachypenia
Cardiovascular Regular rhythm, normal heart Sinus tachycardia, bedside
sounds, and intact distal pulses; echocardiogram grossly
DISCUSSION no gallop; no friction rub; no depressed with left ventricular
Except when pathogens directly enter the murmur heard ejection fraction 5 25%–35%
bloodstream, sepsis occurs in 2 stages: Gastrointestinal Normal bowel sounds, no Vomiting, diarrhea
preseptic and septic. With direct distention, no mass, no
tenderness, no rebound, no
contamination, the preseptic stage is absent15.
guarding
Previously, it was believed the immune system
Urinary UDS ordered
maladaptive response played the predominant Genital All
role in presepsis16,17. New information Vascular All
suggests pathogens are also involved18. Musculoskeletal All
Neurologic LP and EEG planned
Hematologic Comprehensive metabolic panel
Preseptic and Septic Bacterial Role
ordered
The primary sources for bacteria entering the
Endocrine All Thyroid-stimulating hormone and
bloodstream include local infection, lungs, free thyroxine test planned
lymphatics, venous system, or intestines. Only Psychiatric Indeterminate signs/symptoms due to altered mental state
erythrocytes clear bacteria from the
bloodstream19. The erythrocyte membrane is Normal range Measured value
triboelectrically charged to attract bacteria.
Creatinine 0.6–1.2 mg/dL 1.42 mg/dL*
Once fixed to the membrane, oxyhemoglobin Lactate 0.5–1.0 mmol/L 3.4 mmol/L*
is released, killing most bacteria19,20. If a Troponin 0.0–0.04 ng/mL 0.61 ng/mL*
bacterium survives oxidation, it can be trapped
in the concave pocket of an erythrocyte. Once EEG, electroencephalography; LP, lumbar puncture; UDS, urodynamic study.
*Elevated values.
trapped, it is either oxidized and released into

JOE  Volume 47, Number 4, April 2021 Dental Abscess to Septic Shock 665
 plasma for digestion in the reticuloendothelial

planes Thyroid Vasculature

system, released, and removed by the liver and

Normal
Intact
spleen or uses exotoxin to decompose the
erythrocyte membrane and enter the cell15.
Inside an erythrocyte, a bacterium is protected
Normal
from immune complexes and exogenous
antibacterial agents. Using hemoglobin, it can
multiply and rupture the membrane, releasing
Posterior Soft tissue

new bacteria into plasma. This is a critical step

Normal

in developing sepsis15.
Motile and nonmotile bacteria resistant
to host immunity proliferate in tissue and enter
structures:
Visualized

circulation15. Immunity-resistant features

normal
fossa

include superoxide dismutase, catalase, and

gonyautoxin production. These enzymes
convert harmful superoxide to nontoxic water
with Foley catheter in place
Urinary bladder collapsed
and oxygen15. Likewise, a capsule, slime layer,
adrenal glands: normal
and excretion: normal
Kidney enhancement
Paranasal sinuses,

pancreas, spleen,
Liver, gallbladder,
mastoid air cells:

and biofilm protect against phagocytosis, lytic

Other organs/

all well aerated

structures

enzymes, immune complexes, reactive oxygen

species, and erythrocyte attachment20.
Sepsis-causing bacteria must also express a
large quantity/variety of virulence factors and
coordinate individual gene transcription to
maximize virulence potential16.
lesions Osseous

Gram-positive bacteria effectively

Normal

Normal

invade host tissue21 and initiate sepsis via

exotoxins and the exposed cell wall
peptidoglycan22, whereas gram-negative
None
Lytic

bacteria trigger sepsis through

lipopolysaccharide endotoxins23. Most sepsis
involves facultative anaerobic bacteria15, but
mediastinum,
hill, and axilla
Lymph

Normal

Normal

Normal

nonfacultative anaerobes also contribute.

nodes

within

Meanwhile, the bacterial etiology of

endodontic infection is well-documented24.
Endodontic infections contain both gram-
Intracranial

negative and gram-positive facultative and

Normal

obligate anaerobes, with the prevalent phyla

identified as Proteobacteria, Firmicutes,
Bacteroidetes, Fusobacteria, and
TABLE 4 - Findings of Reconstructed Coronal and Sagittal Computed Tomographic Scans

atelectasis, nodules,

Actinobacteria25. Prevotella and

focal consolidation
Lungs: clear; no
vessels: normal
No pericardial
Heart/lungs

apices: clear

Porphyromonas spp. are associated with

Heart/great
Visible lung

or masses
or pleural
effusion

symptomatic infected teeth and are thought to

play an essential role in severe infections26. It is
unknown how many cases of sepsis/septic
shock are the result of dental infections.
When erythrocytes are destroyed by
Free air/

bacteria, inflammation anemia occurs19. With

None

None

None
fluid

no erythrocytes to deliver oxygen to organs,

cell hypoxia results. The kidneys and liver
abdomen endobronchial evidence of
obstruction
Patent, no Normal, no

detect reduced blood oxygen levels and

of ileum
Bowel

secrete erythropoietin to stimulate bone

marrow erythropoiesis. This slightly increases
the blood oxygen transport capacity. Bacterial
attachment to erythrocytes causes premature
Airway

lesions
Patent

oxygen release, platelet activation, and

disseminated intravascular coagulation27,
which provides nutrients for bacterial
proliferation15. Oxidative hormone inactivation
Chest and

leads to muscle wasting and impaired

Head and
neck

wound healing, whereas insulinlike growth

Pelvis

factor inactivation leads to hyperglycemia28.

Lower blood oxidation also affects the

666 Mannan et al. JOE  Volume 47, Number 4, April 2021


FIGURE 2 – The immediate postobturation periapical radiograph. The nonsurgical root canal treatment was completed
by the predoctoral dental student.
hypothalamic-pituitary-thyroid axis, causing
adrenal and vasopressin insufficiency and
thyroid hormone inadequacy. Vasopressin
oxidation along with low levels of angiotensin II
and angiotensin-converting enzyme contribute
to systemic vasodilation29. Resultant albumin
oxidation leads to hypoalbuminemia, which is
identified as an independent predictor of
sepsis mortality15. Lastly, inactivation of
immunoglobulins alters immunoreactivity15.
Preseptic and Septic Host Role
Prolonged overexpression of chemical
mediators required to recruit immune effector
cells evoke harmful biological effects16. Often
referred to as cytokine cascade/dysfunction, it
involves all cell types including antigen-
presenting cells, neutrophils, macrophages,
and lymphocytes. Once the cascade initiates
events, hypoxia and cellular hypoperfusion
lead to transitory organ failure30. Profound
oxidative cellular stress results in
catecholamine depletion, hormonal alterations,
vascular dysfunction, neural dysregulation,
JOE  Volume 47, Number 4, April 2021
and disruptions to immune/metabolic
activities. If the patient is not well managed,
health rapidly deteriorates. Symptoms include
cardiovascular depression, delirium, acute
respiratory distress syndrome, acute renal
failure, and hepatic dysfunction31. A nonlinear,
exponential relationship between cellular injury
and organ failure leads to a high level of
mortality30.
The effect of septic shock on the
cardiovascular system can be divided into 3
major events: vasodilation, maldistribution of
blood flow, and cardiovascular depression31.
Hypotension despite adequate fluid
resuscitation reflects the end of progressive
deterioration17. Myocardial depressant factors
tumor necrosis factor alpha and interleukin 1
beta participate in cardiovascular
depression32. These factors produce
abnormal amounts of nitric oxide and cyclic
guanosine monophosphate. Excessive nitric
oxide leads to decreased vascular resistance,
resulting in maldistribution of blood flow33. It
also interacts with superoxide to form
peroxynitrite, which directly injures intracellular
structures34. Mitochondrial injury limits the
ability of the cytochrome system to generate
adenosine triphosphate, leading to myocardial
depression. Excessive acetylcholine secretion
also leads to myocardial depression, but it can
inhibit tumor necrosis factor alpha expression,
improving survival35.
High concentrations of circulating
catecholamines produced in the early stages
of septic shock enhance the inflammatory
response. Continuous elevated levels result in
depletion, perhaps because of apoptosis of
adrenal medullary cells36. Once depleted, the
patient is predisposed to peripheral
vasodilation, compromised myocardial
contractility, and myocardial depression36.
Hypotension, hypoperfusion, and organ
dysfunction follow. The concomitant abnormal
adrenergic modulation of heart/vessels during
septic shock indicates that adrenergic
regulation impairment contributes to
cardiocirculatory failure36.
Signs and Symptoms of Septic
Shock
Sequential (Sepsis-Related) Organ Function
Assessment (SOFA) scoring is an objective
method to determine dysfunction based on
oxygen levels, platelet count, Glasgow Coma
Scale (GCS) score, bilirubin level, creatinine
level, and mean arterial pressure2. Quick SOFA
(qSOFA) is simpler and predicts death risk2.
One point each is awarded for AMS (GCS
,15), respiratory rate 22 breaths/min, and
systolic blood pressure (BP) 100 mm Hg.
Patients with qSOFA scores of 2–3 are
associated with a 3- to 14-fold increase in
hospital mortality and should be further
assessed with blood testing, including serum
lactate, and full SOFA scoring37. When our
patient suffered from AMS and tachypnea, he
had a qSOFA score of 2.
Our patient presented with serious,
general signs of sepsis including all
components of a toxic appearance38. This
included an ill presentation, shivers/chills,
lethargy, diaphoresis, rapid pulse, and fever of
102 –107 F. Upon arrival to the ED, our
patient was suffering from acute respiratory
failure.
Questioning an infected dental patient
can reveal if he or she is eating or sufficiently
hydrated. Dentists should recognize the signs
and symptoms of dehydration, including a
drawn facial appearance, dry mucous
membranes, fever, loss of skin turgor, oliguria,
postural hypotension, serum electrolyte
changes, thirst, and weakness38. Our patient
was experiencing at least 6 of these signs and
symptoms.
Dental Abscess to Septic Shock 667
 Another symptom of sepsis is central
nervous system changes. Although our patient
was initially alert and oriented, his best eye,
verbal, and motor responses diminished over a
short period of time. Within 30 minutes, his
GCS score was 15, then 11, and then
unresponsive. A declining or “waxing and
waning” GCS is concerning, and the airway
should be reassessed for intervention38. Our
patient was intubated upon arrival in the ED.
Our patient had elevated creatinine
(1.42 mg/dL), lactate (3.4 mmol/L), and
troponin (0.61 ng/mL) values. Elevated
creatinine indicates kidney disease, shock,
dehydration, or congestive heart failure38. The
high lactic acid level was interpreted as
secondary to hypoperfusion, and intravenous
fluid replenishment was continued. Elevated
lactate signals anaerobic metabolism and
indicates sepsis, shock, cardiac arrest, liver
disease, seizure, asthma, trauma, bowel
dysfunction, medication-related damage, or
cancers 38. Troponin values between 0.04 and
0.39 ng/mL may indicate cardiac problems,
with values over 0.4 ng/mL indicating possible
cardiac arrest. Other reasons for elevation
include sepsis, kidney failure, pulmonary
embolism, myocarditis, drug abuse, or
trauma38.
An elevated body temperature highly
predicts acute infection. Moderate to severe
infections always produce an elevated
temperature, whereas a localized acute apical
abscess with or without swelling will not39.
Temperatures .101.3 F indicate simple
pyrexia, whereas hyperthermia is a term
reserved for body temperatures 105.8 F38.
We initially recorded temperatures in our
patient as high as 106 F. Unfortunately, body
temperature was not recorded when the
patient first arrived. If it had been, a referral
could have occurred sooner.
Although there are no or minor changes
in BP during localized infections, sepsis/septic
shock produce significant BP changes
attributed to shock, decreased blood volume,
vasodilatation, or severe dehydration (low BP).
Our 23-year-old patient presented with severe
pain, no known medical conditions, a normal
body mass index of 22.8 kg/m2, and elevated
BP readings that steadily decreased to
hypotension by day 2. The normal
physiological heart rate response to infection
and shock is rapid and weak. Our patient had
recorded rates of 100 beats/min and then 160
beats/min before EMS arrival.
CONCLUSION
Presented is a healthy 23-year-old male whose
condition rapidly deteriorated during an
emergency dental office visit due to sepsis/
septic shock. Significant changes in vital signs
are not expected in localized infections. Hence,
all vital signs should be routinely checked while
examining infected dental patients. BP, pulse,
respiration, and temperature should be
thoughtfully assessed within the context of the
patient’s overall medical and dental conditions
and sudden alterations in mental state,
respiration, and systolic BP quickly acted on.
ACKNOWLEDGMENTS
The authors thank Dr. Michael A. Steinle for his
valuable input.
The authors deny any conflicts of
interest related to this study.

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